Mitochondrial signaling pathway involved in cell apoptosis induced by high fluence low-power laser irradiation

High fluence low-power laser irradiation (HF-LPLI) is a new stimulus to trigger cell apoptosis. Recently, great efforts have been made to investigate the mechanism involved in it. Our results show that HF-LPLI induces cell apoptosis through a large amount of intracellular reactive oxygen species (ROS), especially a higher generation in mitochondria. These triggered ROS causes mitochondrial injury manifested by mitochondrial depolarization and cytochrome c release. Caspase-3 activation is a downstream event which executed cell apoptosis finally. In addition, we exclude caspase-8/Bid signaling pathway in HF-LPLI-induced cell apoptosis. However, another important Bcl-2 pro-apoptotic member Bax participates in the apoptotic process. Our result show that Bax is activated after the diffusion of mitochondrial transmembrane potential and cytochrome c release, suggesting that Bax does not affect outer mitochondrial membrane permeabilization (OMMP). We postulate that the activation of Bax is mediated by oxidative stress caused by laser irradiation through ROS/GSK-3β/Bax pathway. Further studies need to be performed to clarify the exactly mechanism involved in HF-LPLI induced cell apoptosis.